AB1009 INVERSE CORRELATION BETWEEN NONHDL CHOLESTEROL AND INFLAMMATORY BOWEL DISEASE IN SPONDYLOARTHRITIS: A NEW LIPID PARADOX
Authors: J. Rubio Ubeda, A. Peña-Almagro, L. Salvatierra Velasco, E. Raya, J. Salvatierra
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> In Spondyloarthritis (SpA) a higher prevalence of cardiovascular comorbidities has been observed, such as diabetes mellitus (DM), arterial hypertension (AHT), dyslipidaemia (DLP), obesity and metabolic syndrome [1]. In recent years, several studies have established a causal relationship between non-HDL cholesterol (non-HDLC) levels and cardiovascular diseases. Non-HDLC offers a wide vision of proatherogenic lipoproteins containing apolipoprotein B (apoB) -VLDL, IDL, LDL, chylomicron remnants and Lp(a)- without being interfered by triglyceride concentrations. Thus, non-HDLC has become an innovative cardiovascular risk (CVR) biomarker. Therefore, the <i>Multinational Cardiovascular Risk Consortium</i> [2] recently published a set of recommendations estimating CVR based on non-HDLC levels. We have analyzed in a cohort of patients with SpA possible associations between clinic and laboratory data, and non-HDLC serum levels. <h3>Objectives</h3> To analyse in patients with SpA whether there is a relationship between disease-dependent variables (C-reactive protein [CRP] levels, erythrocyte sedimentation rate [ESR], presence of HLA-B27, axial or peripheral involvement, structural damage, and extra-articular manifestations) with non-HDLC serum levels. <h3>Methods</h3> Observational, cross-sectional, single-centre study, which included a sample of 104 patients with both radiographic and non-radiographic SpA, in whom each disease-dependent variable was analyzed individually for its possible association with non-HDLC serum levels. Classical CVR factors were also analyzed. <h3>Results</h3> Of 104 patients included most of them were women (54,8%), mean age was 43 years, 33,7% smoked, HLA-B27 was positive in 52,9% of patients, with mean CRP levels of 9,83 mg/L and ESR of 17,92 mm/h. Axial involvement prevailed over peripheral (92,3% vs 26%). Extra-articular manifestations were distributed as follows: 13,5% uveitis, 7,7% inflammatory bowel disease (IBD) and 4,8% psoriasis. 43,3% of patients had structural damage. None of these patients suffered from cardiovascular disease prior to diagnosis. Regarding the classic CVR factors: AHT was observed in 16,3%, DM in 1.92%, obesity (BMI &gt;30) in 14.4%. Mean non-HDLC was 144.19 mg/dL (± 36,1), giving this population a 12,87% probability of suffering cardiovascular disease at the age of 75. For CVR estimation, we categorized non-HDLC levels according to low (100 - &lt;145 mg/dL), moderate (145 - &lt;185 mg/dL), high (185 - &lt;220) and very high (≥220 mg/dL) levels. Lower mean concentrations of non-HDLC were found in those patients with IBD (117,6 ± 35,7 mg/dL), compared to those without intestinal involvement (146 ± 35,5 mg/dL) (p&lt;0,05). No statistically significant relationships were observed between non-HDLC and the rest of disease-dependent variables. <h3>Conclusion</h3> In our cohort of patients, mean levels of non-HDLC were elevated (144 mg/dL), giving patients a 13% probability of suffering cardiovascular disease at the age of 75. Of clinical and laboratory features analyzed, we observed lower serum concentration of non-HDLC in patients with IBD. This could be explained by lipid malabsorption, as inflammatory damage of the intestinal epithelium decreases the synthesis of apo-B48, which is necessary for both chylomicron formation and hepatic synthesis of apo-B100 [3]. This may turn into lower serum levels of non-HDLC. Therefore, presence of IBD in patients with SpA should be kept in mind when defining non-HDLC levels as an estimator of CVR. <h3>References</h3> [1]Castaneda S, Nurmohamed MT, Gonzlez-Gay MA. Cardiovascular disease in inflammatory rheumatic disease. Best Pract Res Clin Rheumatol. 2016;30: 851-69. [2]Brunner FJ, et al. Application of non-HDL cholesterol for population-based cardiovascular risk stratification: results from the Multinational Cardiovascular Risk Consortium. Lancet. 2019;394(10215):2173–83. [3]Edge SB, Hoeg JM, Schneider PD, Brewer HB Jr. Apolipoprotein B synthesis in humans: liver synthesizes only apolipoprotein B-100. Metabolism. 1985;34(8):726–30. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.